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First published online 14 March 2007
doi: 10.1242/dev.02825

Development 134, 1509-1518 (2007)
Published by The Company of Biologists 2007
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Cell fate polarization in ascidian mesenchyme/muscle precursors by directed FGF signaling and role for an additional ectodermal FGF antagonizing signal in notochord/nerve cord precursors

Gil Jung Kim1,*, Gaku Kumano2 and Hiroki Nishida2

1 Faculty of Marine Bioscience and Technology, Kangnung National University, Gangneung Daehangno, Gangneung 210-702, Republic of Korea.
2 Department of Biological Sciences, Graduate School of Science, Osaka University, Toyonaka, Osaka 560-0043, Japan.

* Author for correspondence (e-mail: gjkim{at}kangnung.ac.kr)

Accepted 31 January 2007

Asymmetric cell division plays a fundamental role in generating various types of embryonic cell. In ascidian embryos, asymmetric cell divisions occur in the vegetal hemisphere in a manner similar to those found in Caenorhabditis elegans. Early divisions in embryos of both species involve inductive events on a single mother cell that result in production of daughters with different cell fates. Here we show in the ascidian Halocynthia roretzi that polarity of muscle/mesenchyme mother precursors is determined solely by the direction from which the FGF9/16/20 signal is presented, a role similar to that of Wnt signaling in the EMS and T cell divisions in C. elegans. However, polarity of nerve cord/notochord mother precursors is determined by possible antagonistic action between the FGF signal and a signal from anterior ectoderm, providing a new mechanism underlying asymmetric cell division. The ectoderm signal suppresses MAPK activation and expression of Hr-FoxA, which encodes an intrinsic competence factor for notochord induction, in the nerve cord lineage.

Key words: Ascidian embryo, Mesenchyme, Notochord, Embryonic induction, Asymmetric cell division, FGF, FoxA


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Asymmetric cell division: fateful FGF antagonism

Development 2007 134: e802. [Full Text]  





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